Ethnicity, Obesity, and Risk of Type 2
Diabetes in Women
A 20-year follow-up study
IRISSHAI,PHD1,2 RUIJIANG,MD3,4 JOANNE. MANSON,MD1,5,6 MEIRJ. STAMPFER,MD1,3,6 WALTERC. WILLETT,MD1,3,6 GRAHAMA. COLDITZ,MD1,6 FRANKB. HU,MD1,3,6OBJECTIVE— To examine ethnic differences in risk of type 2 diabetes, taking dietary and lifestyle risk factors into account.
RESEARCH DESIGN AND METHODS— A prospective (1980 –2000) cohort (from
The Nurses’ Health Study) including 78,419 apparently healthy women (75,584 whites, 801 Asians, 613 Hispanics, and 1,421 blacks) was studied. Detailed dietary and lifestyle information for each participant was repeatedly collected every 4 years.
RESULTS— During 1,294,799 person-years of follow-up, we documented 3,844 incident
cases of diabetes. Compared with whites, the age-adjusted relative risks (RRs) were 1.43 (95% CI 1.08 –1.90) for Asians, 1.76 (1.32–2.34) for Hispanics, and 2.18 (1.82–2.61) for blacks. After adjustment for BMI, the RRs changed to 2.26 (1.70 –2.99) for Asians, 1.86 (1.40 –2.47) for Hispanics, and 1.34 (1.12–1.61) for blacks. For each 5-unit increment in BMI, the multivariate RR of diabetes was 2.36 (1.83–3.04) for Asians, 2.21 (1.75–2.79) for Hispanics, 1.96 (1.93– 2.00) for whites, and 1.55 (1.36 –1.77) for blacks (Pfor interaction⬍0.001). For each 5-kg weight gain between age 18 and the year 1980, the risk of diabetes was increased by 84% (95% CI 58 –114) for Asians, 44% (26 – 63) for Hispanics, 38% (28 – 49) for blacks, and 37% (35– 38%) for whites. A healthy diet high in cereal fiber and polyunsaturated fat and low intransfat and glycemic load was more strongly associated with a lower risk of diabetes among minorities (RR 0.54 [95% CI 0.39 – 0.73]) than among whites (0.77 [0.72– 0.84]).
CONCLUSIONS— The risk of diabetes is significantly higher among Asians, Hispanics, and blacks than among whites before and after taking into account differences in BMI. Weight gain is particularly detrimental for Asians. Our data suggest that the inverse association of a healthy diet with diabetes is stronger for minorities than for whites.
Diabetes Care29:1585–1590, 2006
E
thnic differences in prevalence oftype 2 diabetes are well documented. In 2004, the prevalence of diagnosed diabetes in the U.S. was higher for blacks and Hispanics than for whites across all age-groups (1). For women aged 45– 64 years, the prevalence was 7.8% among
whites, 13.5% among Hispanics, and 15.4% among blacks. From 1980 through 2004, the age-adjusted preva-lence increased by 65% among white women and 37% among black men (1–5). A random sample of 5% of Medicare fee-for-service beneficiariesⱖ65 years of age
(6) showed the prevalence of type 2 dia-betes to be the highest among Hispanics, the lowest among whites, and intermedi-ate for blacks and Asians. The greintermedi-atest in-crease in diabetes prevalence was observed among Asians (68%) during the 7-year period from 1997 to 2004 (6). In a recent population-based national U.S. telephone survey (7), the prevalence of diabetes was significantly higher among Asian Americans than among non-Hispanic whites, after accounting for a lower BMI among Asians.
Diabetes is primarily determined by obesity and lifestyle factors such as diet and exercise (8). However, no previous study has examined whether these factors can explain ethnic differences in preva-lence of diabetes. Therefore, we con-ducted a prospective analysis of ethnic differences in type 2 diabetes risk among 78,419 apparently healthy middle-aged women in the Nurses’ Health Study dur-ing 20 years of follow-up.
A unique feature of this study is the detailed information on diet and lifestyle factors that has been repeatedly obtained during follow-up.
RESEARCH DESIGN AND METHODS
The Nurses’ Health Study population The Nurses’ Health Study cohort was es-tablished in 1976 when 121,700 female registered nurses, aged 30 –55 years and residing in 11 states, completed a mailed questionnaire about their medical history and lifestyle. Follow-up questionnaires have been sent every 2 years to update information on potential risk factors and to identify newly diagnosed cases of can-cer, coronary heart disease, diabetes, and other medical conditions. For the present analysis, we used information from re-spondents to the 1980 questionnaire, when we first inquired about diet. We ex-cluded women who reported a diagnosis of diabetes, cancer, or cardiovascular dis-ease on the 1980 or a previous question-naire. The remaining 78,419 women were followed-up for diabetes incidence
dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-● dur-●
From the1Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts; the 2
Department of Epidemiology, S. Daniel Abraham International Center for Health and Nutrition, Ben-Gurion University, Beer-Sheva, Israel; the3Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts; the4
Department of Medicine, College of Physicians and Surgeons of Columbia University, New York, New York; the5Department of Preventive Medicine, Brigham Women’s Hospital, Boston, Massachusetts; and the6
Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts.
Address correspondence and reprint requests to Iris Shai, RD, PhD, Harvard School of Public Health, Epidemiology, 677 Huntington Ave., Boston, MA 02115. E-mail: [email protected] or frank.hu@ channing.harvard.edu.
Received for publication 9 January 2006 and accepted in revised form 17 April 2006.
A table elsewhere in this issue shows conventional and Syste`me International (SI) units and conversion factors for many substances.
DOI: 10.2337/dc06-0057
© 2006 by the American Diabetes Association.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
ing the subsequent 20 years (1980 – 2000).
Dietary assessment
We used validated semiquantitative food-frequency questionnaires to assess the participants’ diets. Full descriptions of the food-frequency questionnaire in its ab-breviated (61 items: 1980) and expanded (116 –136 items: 1984, 1986, 1990, 1994, and 1998) forms, the procedures for calculating nutrient intakes, and data on reproducibility and validity in this co-hort have been reported previously (9). The glycemic load was calculated by mul-tiplying the grams of carbohydrate in each serving by its glycemic index value. Each unit of dietary glycemic load represents the equivalent effects of 1 g of carbohy-drate from pure glucose (8).
Measurement of nondietary factors In 1980, participants provided informa-tion on their weight and smoking status. We updated this information every 2 years during follow-up. The validity of self-reported weight in this cohort was re-ported previously (r⫽0.96 between self-reported and measured weight) (10). Recalled weight at age 18 years was also highly correlated (r⫽0.87, mean differ-ence with measured weight from the physical examination records for the same age among 118 women [recalled⫺ mea-sured weight]⫽ ⫺1.4 kg) (11).
Information about physical activity was first obtained in 1980 and updated periodically by a validated questionnaire (12). The presence or absence of a family history of diabetes (first-degree) was assessed in 1982 and 1988. Ethnicity was reported in 1992. Participants were classified as white only if they reported being white (i.e., Southern European/ Mediterranean origin, Scandinavian, and other Caucasians). Participants were clas-sified as Asians if they reported that they were Asians other than whites. Partici-pants were considered Hispanic if they re-ported that they were Hispanic other than whites and Asians. Participants were clas-sified as blacks if they reported that they were African American other than the above-mentioned ethnic groups.
Follow-up and ascertainment of incident cases of type 2 diabetes On the baseline and follow-up question-naires mailed every 2 years, we inquired about whether diabetes had been newly diagnosed. When a diagnosis of diabetes was reported, participants were asked to
complete a supplementary questionnaire to confirm the report and to ascertain the date of diagnosis and the details of the diagnostic tests, presenting symptoms, and medications prescribed. After the ex-clusion of women who had type 1 or ges-tational diabetes only, the diagnosis of type 2 diabetes was established if one or more of the following criteria were met:1) one or more classic symptoms (excessive thirst, polyuria, weight loss, or pruritus) plus a fasting plasma glucose concentra-tionⱖ140 mg/dl (7.78 mmol/l) or a ran-dom plasma glucose concentrationⱖ200 mg/dl (11.1 mmol/l), 2) two elevated plasma glucose concentrations on differ-ent occasions (fastingⱖ140 mg/dl [7.78 mmol/l], random ⱖ200 mg/dl [11.1 mmol/l], orⱖ200 mg/dl [11.1 mmol/l] afterⱖ2 h of oral glucose tolerance test-ing) in the absence of symptoms, or3) treatment with medication for hypergly-cemia (insulin or oral hypoglycemic agents). These criteria correspond with those proposed in 1979 by the National Diabetes Data Group (13). In 1997, the fasting plasma glucose concentration in-dicative of type 2 diabetes was lowered (ⱖ126 mg/dl [7.0 mmol/l]) (14). Here we used the previous criterion because the National Diabetes Data Group definition was the standard during most of the fol-low-up period. The high validity of self-reported diabetes in this cohort on the supplementary questionnaire was previ-ously documented, and the diagnosis was confirmed by a review of medical records in 98% of cases (15).
Statistical analysis
For each participant, person-time of fol-low-up was counted from the date of re-turn of the 1980 questionnaire to the date of diabetes diagnosis, the return of the most recent follow-up questionnaire, or 1 June 2000, whichever came first. We used general linear models to compare the age-adjusted means and proportions of the population baseline characteristic across the ethnic groups. We conducted Cox proportional hazard analysis stratified on 5-year age categories and over each 2-year follow-up interval to estimate the relative risks (RRs) of diabetes. To evaluate whether obesity explained ethnic differ-ences in diabetes risk, we first added BMI values as a continuous variable (updated every 2 years) to the age-adjusted model. Subsequently, we tested a multivariable model by further adjusting for family his-tory of diabetes in a first-degree relative, smoking status, physical activity, and
al-cohol intake. We further adjusted for di-etary score and total energy intake. The dietary score was calculated as the sum of the quintile values of cereal fiber and the ratio of polyunsaturated to saturated fats in ascending order and oftransfats and glycemic load in descending order (9). We evaluated the contribution of BMI (in 5-unit increments) to diabetes incidence among each ethnic group in stratified analyses. The test for interaction was per-formed using the likelihood ratio test for nested models with and without interac-tion terms for ethnicity and BMI (16). All statistical analyses were performed with SAS statistical software version 8.0 (SAS Institute, Cary, NC).
RESULTS— Table 1 shows age-ad-justed baseline characteristics of 78,419 women across the ethnic groups. Blacks were heavier, more sedentary, and had a higher prevalence of hypertension than whites. Hispanics had risk-factor patterns similar to those of whites, except for a lower prevalence of smoking. Asians were leaner than whites but more sedentary, had a lower prevalence of smoking, and tended to consume less alcohol and to eat a healthier diet, as assessed by our dietary score.
During 20 years of follow-up (1,294,799 person-years), we docu-mented 3,844 incident cases of type 2 di-abetes. In age-adjusted models (Table 2), minority groups, especially blacks, had significantly higher risk of diabetes than whites. Further adjustment for updated BMI attenuated the RR among the blacks to 1.34 (95% CI 1.12–1.61) and appre-ciably increased the RR among Asians to 2.26 (1.70 –2.99). Adjustment for BMI did not materially change the RR of type 2 diabetes among Hispanics. Further ad-justment for family history of diabetes, al-cohol intake, smoking status, and physical activity only slightly attenuated these RRs. Additional adjustments for up-dated dietary score and energy intake did not appreciably alter these RRs.
During the 20 years of follow-up, BMI increased across all the ethnic groups (Fig. 1). In multivariate analyses, for each 5-unit increment in BMI, the RRs of dia-betes were 2.36 (95% CI 1.83–3.04) for Asians, 2.21 (1.75–2.79) for Hispanics, 1.96 (1.93–2.00) for whites, and 1.55 (1.36 –1.77) for blacks (Pfor interaction between BMI and ethnicity⬍0.001) (Ta-ble 3). We further evaluated weight change between age 18 years and the year 1980 in relation to incidence of diabetes
between 1980 and 2000 (Table 3). Weight gain since age 18 years was the lowest among Asians (mean 5.5 kg) and the highest among blacks (mean 13.4 kg). In a multivariate model including BMI at age 18 years, weight gain during adult-hood appeared to be most strongly asso-ciated with diabetes in Asians; for each 5-kg increment in weight gain since age 18 years, the RR of diabetes was 1.84 (1.58 –2.14) for Asians, 1.44 (1.26 –1.63) for Hispanics, 1.38 (1.28 –1.49) for blacks, and 1.37 (1.35–1.38) for whites
(all P values ⬍0.05 comparing Asians with each of the other ethnic groups).
We attempted to examine the associ-ations between other risk factors (dietary score, alcohol, and family history of dia-betes) and risk of diabetes for each ethnic group. The directions of the associations between these variables and diabetes were generally similar for the minority groups, but the 95% CIs were wide because of the relatively small number of diabetes cases. Thus, we combined the three minority groups. In the combined analyses
adjust-ing for age, BMI, ethnicity, and other co-variates, a higher diet score (above median) was more strongly associated with a lower risk of diabetes among mi-norities (RR 0.54 [95% CI 0.39 – 0.73]) than among whites (0.77 [0.72– 0.84]). Moderate alcohol intake (5 g or more per day) was equally beneficial among minor-ities (0.64 [0.40 –1.02]) and whites (0.64 [0.58 – 0.70]). Family history of diabetes was associated with a higher risk of dia-betes among both minorities (2.17 [1.66 – 2.84]) and whites (2.44 [2.29 –2.61]). Table 1—Age-adjusted diabetes-related risk factors of 78,419 women without diabetes at baseline (1980) across ethnic groups
Ethnic group
White* Asian Hispanic Black
n 75,584 801 613 1,421
Age (years) 45.7 45.9 46.2 46.1
BMI (kg/m2) 24.3⫾4.4 22.7⫾0.43† 24.3⫾4.0 26.0⫾5.3†
Parental history of diabetes (%) 17.1 21.1‡ 21.4‡ 17.7
Moderate/vigorous exercise (h/week) 4.0⫾2.7 3.4⫾3.7† 3.8⫾4.2 3.4⫾3.8†
Current smoker (%) 28.2 14.6† 15.1† 25.9
Hypertension (%) 14.0 13.4 10.4‡ 28.1†
Hypercholesterolemia (%) 4.6 6.5‡ 5.4 4.9
Alcohol consumption (g/day) 6.5⫾10.4 2.6⫾8.1† 4.7⫾14.6‡ 4.3⫾12.8
Polyunsaturated fat (% energy) 5.3⫾1.56 5.0⫾1.4† 4.8⫾0.2† 5.1⫾3.8†
Saturated fat (% energy) 15.6⫾3.5 14.5⫾3.9† 15.2⫾5.0‡ 14.0⫾3.8†
Polyunsaturated-to-saturated fat ratio 0.4⫾0.1 0.4⫾0.2† 0.3⫾0.02‡ 0.4⫾0.4†
Transfat (% energy) 2.2⫾0.7 1.9⫾0.6† 2.0⫾0.02† 1.9⫾0.4†
Total fat intake (% energy) 39.0⫾8.2 37.6⫾9.3† 37.9⫾10.9‡ 36.3⫾9.8†
Cereal fiber (g/day) 12.2⫾4.5 11.0⫾4.1 8.7⫾2.2† 7.4⫾3.8†
Total crude fiber intake (g/day) 53.5⫾1.5 55.2⫾1.7 73.7⫾2.0† 55.1⫾1.8‡
Glycemic load 121⫾35.3 132⫾36.3† 124⫾49.5 137⫾45.2†
Dietary score§ 6.2⫾2.7 6.4⫾0.3‡ 6.2⫾2.5 6.1⫾3.7
Magnesium (mg/day) 295⫾69.9 282⫾69.0† 293⫾71.5 271⫾86.7†
Caffeine (mg/day) 395⫾302 345⫾11.5† 335⫾379† 269⫾336†
Total energy intake (kcal/day) 1,571⫾492 1,617⫾561‡ 1,561⫾698 1,578⫾622 Data are means⫾SD unless otherwise indicated. *Includes those with Southern European/Mediterranean ancestry, Scandinavian ancestry, and other Caucasian ancestry. ‡P⬍0.05, †P⬍0.0001 as compared with whites. §The dietary score is the sum of quintile values (0 – 4) for cereal fiber, ratio of polyunsaturated fat to saturated fat (ascending order), glycemic load, andtransfat (descending order). A higher score indicates a healthier diet.
Table 2—RR (95% CI) of type 2 diabetes associated with ethnicity during 20 years of follow-up among 78,419 women
Ethnic group
White Asian Hispanic Black
n 75,584 801 613 1,421
Person-years of follow-up 1,254,454 11,671 9,248 19,427
Incident cases of diabetes 3,624 49 48 123
Age adjusted 1.0 (ref.) 1.43 (1.08–1.90) 1.76 (1.32–2.34) 2.18 (1.82–2.61) Age and BMI adjusted 1.0 (ref.) 2.26 (1.70–2.99) 1.86 (1.40–2.47) 1.34 (1.12–1.61) Multivariate* 1.0 (ref.) 1.94 (1.46–2.58) 1.70 (1.28–2.26) 1.36 (1.14–1.63) Additional adjustment for dietary score†
and energy intake
1.0 (ref.) 1.99 (1.50–2.64) 1.73 (1.30–2.31) 1.38 (1.15–1.66) *Adjusted for age (5-year categories), BMI (continuous), family history of diabetes, alcohol intake (none, 0.1– 4.9, 5–14.9, and 15⫹g/day), smoking status (never, past smoker, current 1–14, current 15–24, and current 25⫹cigarettes/day), and moderate/vigorous exercise (0 – 0.9, 1–1.9, 2–3.9, 4 – 6.9, and 7⫹h/week) (updated variables). †The dietary score is the sum of quintile values for cereal fiber, ratio of polyunsaturated fat to saturated fat (ascending order), glycemic load, andtransfat (descending order). A higher score indicates a healthier diet (updated variables).
CONCLUSIONS— In this 20-year prospective study, Asians, Hispanics, and blacks all had a significantly higher risk of type 2 diabetes than whites after control-ling for BMI. Our data suggest that a diet high in cereal fiber and polyunsaturated fat and low intransfat and glycemic load appears to have a stronger inverse
associ-ation with diabetes risk among the minor-ities than among whites.
The strengths of our study include the large sample size, long follow-up, and detailed and repeated ascertainment of dietary and lifestyle measurements. However, some limitations of our study warrant consideration. We had no
infor-mation about specific countries of origin, a variable that represents genetic and cul-tural factors within each ethnic group. We also had no information about length of residence in the U.S. A recent study showed that residency of immigrants in the U.S. for longer than 10 years was as-sociated with increased obesity (17). However, our analyses took into account both baseline and current BMI levels in different ethnic groups. Even though we controlled for several major diabetes risk factors in the analyses, we cannot exclude the possibility of unmeasured confounders. The participants are predominantly white women, reflecting the ethnic background of women who trained as registered nurses through the 1960s. However, the cohort provides important data on diet and lifestyle across different ethnic groups. Finally, al-though this cohort is not a random sample of U.S. women, the relative socioeconomic homogeneity of the cohort can reduce the impact of unknown confounders.
In the Third National Health and Nu-trition Examination Survey, the preva-lence rates of diabetes for non-Hispanic blacks were 1.6 times the rate for non-Hispanic whites (3). In our cohort, the age-adjusted RR of type 2 diabetes among blacks was more than twice that in whites. However, the increased risk was attenu-ated after adjustment for BMI. In general, BMI was much higher among blacks than among whites, but its contribution to di-abetes risk was lower among blacks. Stud-Figure 1—Age-adjusted means of BMI during 20 years of follow-up among 78,419 women by
ethnic group.
Table 3—RR (95% CI) of type 2 diabetes associated with a 5-unit increment in BMI during follow-up (1980 –2000) and with a 5-kg increment in weight between age 18 years and the year 1980 among 78,419 women, stratified by ethnic group
Ethnic groups
White Asian Hispanic Black
n 75,584 801 613 1,421
Person-years of follow-up 1,254,454 11,671 9,248 19,427
Incident cases of diabetes 3,624 49 48 123
Change of BMI between 1980–2000 RR of BMI change (increments of 5 units,
multivariate model)*
1.96 (1.93–2.00)a 2.36 (1.83–3.04)a 2.21 (1.75–2.79)a 1.55 (1.36–1.77)b
Change of weight between age 18 years and the year 1980
Weight at age 18 years (kg) 57.3⫾8.5 50.6⫾7.4 53.4⫾7.8 55.8⫾8.2 BMI at age 18 years (kg/m2) 21.3⫾2.9 20.3⫾2.6 20.7⫾2.7 20.8⫾3.1
Weight change since age 18 years until 1980 (kg)
7.6⫾9.9 5.5⫾7.6 8.8⫾9.0 13.4⫾10.9
RR of weight change (increments of 5 units), multivariate model†
1.37 (1.35–1.38)a 1.84 (1.58–2.14)b 1.44 (1.26–1.63)a 1.38 (1.28–1.49)a *Adjusted for age (5-year categories), family history of diabetes, alcohol intake (⬍/ⱖ5 g/day), smoking status (current/noncurrent), moderate/vigorous exercise (0, 1–2, and 3⫹h/week), and dietary score (below/above median). †Adjusted for age (5-year categories), BMI at age 18 (continuous), family history of diabetes, alcohol intake (⬍/ⱖ5 g/day), smoking status (current/non-current), moderate/vigorous exercise (0, 1–2, and 3⫹h/week), and dietary score (below/above median) (updated variables).a, bDifferent letters indicate significant differences between groups.
ies have demonstrated greater visceral adipose tissue in whites than in blacks de-spite the greater amount of total body fat in black women than in white women (18 –19). However, black obese women demonstrate a higher degree of insulin re-sistance than white obese women despite less visceral fat (20).
Several studies have documented in-creased prevalence of diabetes among Asian-American immigrants (21,22). In contrast to white diabetic patients, whose BMIs are much higher than those of indi-viduals without diabetes, the BMIs of both Japanese (23) and Thai (24) diabetic co-horts are often not in the obesity range as defined for Western populations. Our re-sults suggest that the association between obesity and diabetes was more evident among Asian women than women in other ethnic groups. Previous studies have demonstrated a strong relationship between BMI and cardiovascular risk fac-tors in Asian populations (25), although the range of BMI is at the lower end of the distribution for typical western popula-tions. Recent studies suggest that lower cutoff BMI values for classifying over-weight and obesity status are needed to identify Asians at a higher risk of cardio-vascular disease and diabetes because Asians tend to have a higher percentage of body fat (26), particularly abdominal vis-ceral fat (27), than whites with the same BMI.
The age-adjusted diabetes prevalence among U.S. Hispanics during 1998 – 2002 was approximately twice that among non-Hispanic whites (9.8 vs. 5.0%), as reported by the Centers for Dis-ease Control and Prevention (28). Also, at each BMI level, the prevalence of type 2 diabetes among Hispanics was higher than among non-Hispanic whites (28). In the San Antonio Heart Study, the inci-dence of type 2 diabetes among Mexican Americans tripled during the 7– 8 years of follow-up. The trend remained significant after adjusting for obesity and other risk factors (29). The RR of diabetes among Hispanics was not attenuated after con-trolling for BMI and several risk factors, suggesting that other factors may account for the increased risk of diabetes among Hispanics.
Our study suggests that ethnic differ-ences in diabetes risk are only partially explained by differences in known diabe-tes risk factors. So far, the biological basis for the ethnic differences has not been fully elucidated. In metabolic studies, postprandial glucose was markedly
higher in Asians than in whites (30). Spe-cifically, among lean, healthy subjects matched for age, BMI, waist circumfer-ence, birth weight, and current diet, Asians (especially those of Southeast Asian descent) had significantly higher postprandial glycemia and lower insulin sensitivity than whites in response to a 75-g carbohydrate load. In several epide-miologic studies, Asians (31), blacks (31,32), and Mexican Americans (32) were found to be less insulin-sensitive than non-Hispanic whites after adjusting for obesity. These findings suggest that reduced insulin sensitivity may underlie the increased risk of type 2 diabetes in minorities in the U.S., especially among Asians. Because insulin sensitivity is de-termined partly by genetic factors, one could infer that the racial/ethnic differ-ences in diabetes risk are attributed to genetic predisposition. However, adjust-ment for family history of diabetes did not appear to alter the risk estimates for dif-ferent ethnic groups, and genetic factors alone would not explain the marked in-crease in prevalence of type 2 diabetes during the past decade. We speculate that the observed ethnic difference in diabetes risk is likely due to an interaction between diet and lifestyle and increased genetic susceptibility among minorities.
In our study, the diet score (repre-senting a higher intake of fiber and poly-unsaturated-to-saturated ratio and a lower glycemic load and intake oftrans fat) was more strongly associated with di-abetes risk among minorities than whites. These results suggest that dietary inter-vention may be particularly effective for diabetes prevention among minorities, al-though this hypothesis needs to be tested in future studies.
In conclusion, after accounting for BMI, our study indicates that Asians, His-panics, and blacks were all at higher risk for type 2 diabetes than whites. The asso-ciation between increasing BMI and greater weight gain and risk of diabetes was most pronounced among Asians, suggesting that lower cutoff BMI values are needed to identify Asians at a higher risk of diabetes.
Acknowledgments— We acknowledge the continued dedication of the participants in the study. This study was supported by National Institutes of Health Grants DK58845, P30 DK46200, and CA87969. I.S. was supported by the Fulbright Foundation, USA, and by the S. Daniel Abraham International Center for Health and Nutrition, Ben-Gurion University
of the Negev. F.B.H. is partly supported by American Heart Association Established In-vestigator Award.
References
1. The National Center for Chronic Disease Prevention and Health Promotion: Age-specific prevalence of diagnosed diabetes, by race/ethnicity and sex, United States [article online], 2004. Available at http:// www.cdc.gov/diabetes/statistics/prev/na-tional/fig2004.htm. Accessed 13 March 2005
2. Bolen JC, Rhodes L, Powell-Griner EE, Bland SD, Holtzman D: State-specific prevalence of selected health behaviors, by race and ethnicity: Behavioral Risk Factor Surveillance System, 1997.MMWR CDC Surveill Summ49:1– 60, 2000
3. Harris MI, Flegal KM, Cowie CC, Eber-hardt MS, Goldstein DE, Little RR, Wied-meyer HM, Byrd-Holt DD: Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults: the Third National Health and Nutrition Examination Survey, 1988 –1994. Diabe-tes Care21:518 –524, 1998
4. Lipton RB, Liao Y, Cao G, Cooper RS, Mc-Gee D: Determinants of incident non–in-sulin-dependent diabetes mellitus among blacks and whites in a national sample: the NHANES I Epidemiologic Follow-up Study. Am J Epidemiol 138:826 – 839, 1993 [erratum inAm J Epidemiol139:964, 1994]
5. Brancati FL, Kao WH, Folsom AR, Watson RL, Szklo M: Incident type 2 dia-betes mellitus in African American and white adults: the Atherosclerosis Risk in Communities Study. JAMA 283:2253– 2259, 2000
6. McBean AM, Li S, Gilbertson DT, Collins AJ: Differences in diabetes prevalence, in-cidence, and mortality among the elderly of four racial/ethnic groups: whites, blacks, Hispanics, and Asians. Diabetes Care27:2317–2324, 2004
7. McNeely MJ, Boyko EJ: Type 2 diabetes prevalence in Asian Americans: results of a national health survey.Diabetes Care27: 66 – 69, 2004
8. Hu FB, Manson JE, Stampfer MJ, Colditz G, Liu S, Solomon CG, Willett WC: Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. N Engl J Med 345: 790 –797, 2001
9. Willett WC, Sampson L, Browne ML, Stampfer MJ, Rosner B, Hennekens CH, Speizer FE: The use of a self-administered questionnaire to assess diet four years in the past. Am J Epidemiol127:188 –199, 1988
10. Willett W, Stampfer MJ, Bain C, Lipnick R, Speizer FE, Rosner B, Cramer D, Hen-nekens CH: Cigarette smoking, relative weight, and menopause.Am J Epidemiol
11. Troy LM, Hunter DJ, Manson JE, Colditz GA, Stampfer MJ, Willett WC: The valid-ity of recalled height and past weight among younger women. Int J Obes 19: 570 –572, 1995
12. Hu FB, Sigal RJ, Rich-Edwards JW, Cold-itz GA, Solomon CG, Willett WC, Speizer FE, Manson JE: Walking compared with vigorous physical activity and risk of type 2 diabetes in women: a prospective study.
JAMA282:1433–1439, 1999
13. National Diabetes Data Group: Classifica-tion and diagnosis of diabetes mellitus and other categories of glucose intoler-ance.Diabetes28:1039 –1057, 1979 14. Expert Committee on the Diagnosis and
Classification of Diabetes Mellitus: Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus.
Diabetes Care20:1183–1197, 1997 15. Manson JE, Rimm EB, Stampfer MJ,
Cold-itz GA, Willett WC, Krolewski AS, Rosner B, Hennekens CH, Speizer FE: Physical activity and incidence of non-insulin-de-pendent diabetes mellitus in women. Lan-cet338:774 –778, 1991
16. Flanders WD, Rothman KJ: Interaction of alcohol and tobacco in laryngeal cancer.
Am J Epidemiol115:371–379, 1982 17. Goel MS, McCarthy EP, Phillips RS, Wee
CC: Obesity among US immigrant sub-groups by duration of residence. JAMA
292:2860 –2867, 2004
18. Lovejoy JC, de la Bretonne JA, Lemperer M, Tulley R: Abdominal fat distribution and metabolic risk factors: effects of race.
Metabolism45:1119 –1124, 1996 19. Hill JO, Sidney S: Lewis CE, Tolan K,
Scherzinger AL, Stamm ER: Racial dif-ferences in amounts of visceral adipose tissue in young adults: the CARDIA (Coronary Artery Risk Development in
Young Adults) study.Am J Clin Nutr69: 381–387, 1999
20. van der Merwe MT, Crowther NJ, Schla-phoff GP, Gray IP, Joffe BI, Lonnroth PN: Evidence for insulin resistance in black women from South Africa.Int J Obes Relat Metab Disord24:1340 –1346, 2000 21. Hosler AS, Melnik TA: Prevalence of
diag-nosed diabetes and related risk factors: Japanese adults in Westchester County, New York.Am J Public Health93:1279 – 1281, 2003
22. Nakagami T, Qiao Q, Carstensen B, Nhr-Hansen C, Hu G, Tuomilehto J, Balkau B, Borch-Johnsen K, The DECODE-DE-CODA Study Group: Age, body mass index and type 2 diabetes-associations modified by ethnicity.Diabetologia 46: 1063–1070, 2003
23. Sone H, Ito H, Ohashi Y, Akanuma Y, Yamada N, Japan Diabetes Complication Study Group: Obesity and type 2 diabetes in Japanese patients (Letter).Lancet361: 85, 2003
24. Aekplakorn W, Stolk RP, Neal B, Suriya-wongpaisal P, Chongsuvivatwong V, Cheepudomwit S, Woodward M, IN-TERASIA Collaborative Group: The prev-alence and management of diabetes in Thai adults: the international collabora-tive study of cardiovascular disease in Asia.Diabetes Care26:2758 –2763, 2003 25. Hu FB, Wang B, Chen C, Jin Y, Jang J, Stampfer MJ, Xu X: Body mass index and cardiovascular risk factors in a rural Chi-nese population.Am J Epidemiol151:88 – 97, 2000
26. Deurenberg-Yap M, Deurenberg P: Is a re-evaluation of WHO body mass index cut-off values needed? The case of Asians in Singapore.Nutr Rev61:S80 –S87, 2003 27. Tanaka S, Horimai C, Katsukawa F:
Eth-nic differences in abdominal visceral fat accumulation between Japanese, African-Americans, and Caucasians: a meta-anal-ysis. Acta Diabetol 40 (Suppl. 1):S302– S304, 2003
28. Centers for Disease Control and Preven-tion (CDC): Prevalence of diabetes among Hispanics: selected areas, 1998 –2002.
MMWR Morb Mortal Wkly Rep 53: 941–944, 2004
29. Burke JP, Williams K, Gaskill SP, Hazuda HP, Haffner SM, Stern MP: Rapid rise in the incidence of type 2 diabetes from 1987 to 1996: results from the San Anto-nio Heart Study. Arch Intern Med
159:1450 –1456, 1999
30. Dickinson S, Colagiuri S, Faramus E, Pe-tocz P, Brand-Miller JC: Postprandial hyperglycemia and reduced insulin sensi-tivity differ among lean young adults of different ethnicities. J Nutr 132:2578 – 2583, 2002
31. Torrens JI, Skurnick J, Davidow AL, Ko-renman SG, Santoro N, Soto-Greene M, Lasser N, Weiss G: Ethnic differences in insulin sensitivity and-cell function in premenopausal or early perimenopausal women without diabetes: the Study of Women’s Health Across the Nation (SWAN). Diabetes Care 27:354 –361, 2004
32. Haffner SM, D’Agostino R, Saad MF, Re-wers M, Mykkanen L, Selby J, Howard G, Savage PJ, Hammer RF, Waganknecht LE: Increased insulin resistance and insulin secretion in nondiabetic African-Ameri-cans and Hispanics compared with non-Hispanic whites: the Insulin Resistance Atherosclerosis Study.Diabetes 45:742– 748, 1996